King B M, Arceneaux E R, Cook J T, Benjamin A L, Alheid G F
Department of Psychology, University of New Orleans, LA 70148, USA.
Physiol Behav. 1996 Apr-May;59(4-5):843-8. doi: 10.1016/0031-9384(95)02146-9.
Bilateral lesions centered in the posterodorsal amygdala of female rats resulted in hyperphagia and excessive weight gain (mean = 65.3 g in 20 days compared to 6.8 g for control animals). The brain damage always extended posteriorly into the ventral hippocampal formation. However, lesions that were confined to the ventral hippocampus or amygdalohippocampal area had no effect on daily food intake or body weight, nor did lesions at any other hippocampal site. In a previous study, lesions of the basolateral, corticomedial, and anterior groups of amygdaloid nuclei failed to affect food intake or body weight. It is concluded that the posterodorsal aspect of the amygdala is the critical site for this experimentally induced obesity syndrome. New coordinates for the effective site are presented.
以雌性大鼠杏仁核后背部为中心的双侧损伤导致食欲亢进和体重过度增加（20天内平均增加65.3克，而对照动物为6.8克）。脑损伤总是向后延伸至腹侧海马结构。然而，局限于腹侧海马或杏仁核 - 海马区域的损伤对每日食物摄入量或体重没有影响，海马其他任何部位的损伤也没有影响。在先前的一项研究中，杏仁核基底外侧、皮质内侧和前部组的损伤未能影响食物摄入量或体重。得出的结论是，杏仁核的后背部是这种实验性诱导肥胖综合征的关键部位。给出了有效部位的新坐标。
